Immunohistochemical Expression of Cyclin B1 in Epithelial Hyperplasia, Dysplasia and Oral Squamous Cell Carcinomas - A Comparative Study

摘要

Introduction: Cyclin B1 is important in the cell cycle progression from G2 to M phase. Cyclin B1 binds to CDC2, which then becomes dephosphorylated and gets relocated to the nucleus, ensuring the transition toward mitosis.Aim: Over expression of Cyclin B1, has been reported more recently in breast, colon, prostate, oral and esophageal carcinomas. Thus, the aim of the present study was to examine the expression of Cyclin B1 in hyperplasia, dysplasia and Oral Squamous Cell Carcinomas (OSCC).Materials and Methods: A total of 64 histopathologically diagnosed cases of epithelial hyperplasias, dysplastic oral epithelium and OSCC were included in the study. Immunohistochemical procedure was carried out using the monoclonal mouse Cyclin B1 antibody (Clone V-152). The Cyclin B1 positive tumor cells counted were expressed as percentage of positive tumor cells. Nuclear and cytoplasmic labeling index (n&cLI) were calculated. The results were tabulated and statistically analyzed by Kruskal Wallis test- One Way ANOVA and Mann Whitney U- test.Results: Combined n&cLI was considered only 28.57% of epithelial hyperplasias, 40.7% of oral epithelial dysplasias and 72% of OSCC showed over expression of Cyclin B1 with p value being 0.029. Cyclin B1 expression was not significantly different between the grades of dysplasia, between the grades of OSCC and between the marginal groups.Conclusion: The present study demonstrates more than 50% of the study group showing less than 20% of nuclear staining. The importance of such variations within a type of lesion requires further investigation, since Cyclin B1 has proved useful in many studies from esophageal and laryngeal squamous cell carcinoma as a prognostic indicator, an indicator of recurrence and as an indicator for tumor sensitivity to radiotherapy. Further studies are to be extended towards evaluating the role of Cyclin B1 as a prognostic indicator.